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机构地区:[1]第一军医大学福总临床医学院消化内科,福州350025 [2]南京军区福州总医院消化内科,福州350025
出 处:《福建医科大学学报》2006年第1期26-29,共4页Journal of Fujian Medical University
基 金:福建省青年科技人才创新基金资助项目(2002J059)
摘 要:目的探讨环氧合酶-2(COX-2)表达在Barrett食管(BE)及食管腺癌(EA)发生发展中的作用及COX-2抑制剂在预防与治疗BE及EA中的作用。方法170只SD大鼠分为无反流组、铁剂组、反流组、反流铁剂组、塞来昔布组5组,手术制作胃食管反流模型。术后铁剂组、反流铁剂组与塞来昔布组大鼠腹腔注射右旋糖苷铁(50mg/kg,每周2次,共22周),同时塞来昔布组予以塞来昔布(20 mg.kg-1.d-1)灌胃,共22周。24周后取得食管标本,病理检查大鼠食管BE及EA的发生情况,应用SP免疫组织化学染色检测COX-2的表达活性。结果无反流组与无反流铁剂组未发生BE、异型增生和EA,反流铁剂组BE、异型增生及EA的发生率高于反流组与塞来昔布组(P<0.05)。反流铁剂组免疫组织化学染色COX-2阳性率及阳性程度高于其他组(P<0.05),塞来昔布组与反流组比较差别无统计学意义(P>0.05)。COX-2在肿瘤中表达最高,异型增生中次之,正常黏膜表达最低。结论COX-2表达的增加可能与BE及EA的发生发展有关;选择性COX-2抑制剂能减少动物模型BE及EA的发生率。Objective To study the effect of cyclooxygenase 2(COX-2) and its selective inhibitors on Barrett's esophagus(BE) and esophageal adenocarcinoma(EA) in animal model. Methods 170 Sprague-Dawley rats were randomized into 5 groups: nonreflux group, iron(Fe) group, reflux group, reflux adding iron group and celecoxib group. Model of gastroesophageal reflux was performed by. After 2 weeks, iron dextran were injected intraperitoneum of the rats in Fe group, reflux adding iron group and celecoxib group (50 mg/kg, twice per week for 22 weeks). At the same time, celecoxib(20 mg·kg^-1· d^-1) was given to rats in celecoxib group. At 24 weeks all esophageal samples were taken by operation. All esophagi were assessed for presence of cancer, BE, and dysplasia by gross and microscopy observation. COX-2 expression was examined in all groups by immunohistochemical staining of SP. Results There are no BE, dysplasia and EA in former two groups. The incidence of BE, dysplasia and EA of reflux adding iron group were significantly higher than those of reflux group( P 〈 0.05 ) and celecoxib group( P 〈 0.05). The levels of COX-2 expression in reflux adding iron group were significantly greater than other group and that was no differents between Celecoxib group and reflux adding iron group(P 〉0.05). The expressions were the strongest in EA.Conclusion Increasing express of COX-2 may be associated with the development of BE and EA. This provides evidence that selective COX-2 inhibitors may have preventive potential in BE and EA.
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